Myocardial "stunning" is characterized by a reversible postischemic contractile dysfunction despite full restoration of blood flow. The underlying mechanisms are not clearly understood. Inadequate energy supply and impaired sympathetic neurotransmission may have been excluded. Potential mechanisms, which are not mutually exclusive, may include damage to membranes and enzymes by free radicals, an increase in free cytosolic calcium during ischemia and reperfusion, and a lower calcium sensitivity of myofibrils. The equally pronounced increases in regional contractility in normal and stunned myocardium during postextrasystolic potentiation and the infusion of calcium or the calcium-sensitizing agent AR-L-57, however, suggest an unchanged calcium sensitivity in reperfused myocardium. Pretreatment with calcium antagonists before ischemia attenuates myocardial stunning. This effect is probably related to a lessened myocardial calcium overload during early ischemia. The potential benefit of treatment with calcium antagonists after reperfusion is established remains controversial.